The heart is a muscular organ comprising multiple chambers that operate in concert to circulate blood throughout the body's circulatory system. As shown in FIG. 1, the heart 100 includes a right-side portion or pump 102 and a left-side portion or pump 104. The right-side portion 102 includes a right atrium 106 and a right ventricle 108. Similarly, the left-side portion 104 includes a left atrium 110 and a left ventricle 112 separated by an interventricular septum 105. Oxygen-depleted blood returning to the heart 100 from the body collects in the right atrium 106. When the right atrium 106 fills, the oxygen-depleted blood passes into the right ventricle 108 where it can be pumped to the lungs (not shown”) via the pulmonary arteries 117.
Within the lungs, waste products such as carbon dioxide are removed from the blood and expelled from the body and oxygen is transferred to the blood. Oxygen-rich blood returning to the heart 100 from the lungs via the pulmonary veins (not shown) collects in the left atrium 110. The circuit between the right-side portion 102, the lungs, and the left atrium 110 is generally referred to as the pulmonary circulation. After the left atrium 110 fills, the oxygen-rich blood passes into the left ventricle 112 where it can be pumped throughout the entire body. In so doing, the heart 100 is able to supply oxygen to the body and facilitate the removal of waste products from the body.
To circulate blood throughout the body's circulatory system as described above, a beating heart performs a cardiac cycle that includes a systolic phase and a diastolic phase. During the systolic phase, or systole, the ventricular muscle cells of the right and left ventricles 108 and 112 contract to pump blood through the pulmonary circulation and throughout the body, respectively. Conversely, during the diastolic phase, or diastole, the ventricular muscle cells of the right and left ventricles 108 and 112 relax, during which the right and left atriums 106 and 110 contract to force blood into the right and left ventricles 108 and 112, respectively. Typically, the cardiac cycle occurs at a frequency between 60 and 100 cycles per minute and can vary depending on physical exertion and/or emotional stimuli, such as pain or anger.
The contractions of the muscular walls of each chamber of the heart 100 are controlled by a complex conduction system that propagates electrical signals to the heart muscle tissue to effectuate the atrial and ventricular contractions necessary to circulate the blood. As shown in FIG. 2, the complex conduction system includes an atrial node 120 (the sinoatrial node) and a ventricular node 122 (the atrioventricular node). The sinoatrial node 120 initiates an electrical impulse that spreads through the muscle tissues of the right and left atriums 106 and 110 and the atrioventricular node 122. As a result, the right and left atriums 106 and 110 contract to pump blood into the right and left ventricles 108 and 112, as discussed above.
At the atrioventricular node 122, the electrical signal is momentarily delayed before propagating through the right and left ventricles 108 and 112. Within the right and left ventricles 108 and 112, the conduction system includes right and left bundle branches 126 and 128 that extend from the atrioventricular node 122 via the Bundle of His 124. The electrical impulse spreads through the muscle tissues of the right and left ventricles 108 and 112 via the right and left bundle branches 126 and 128, respectively. As a result, the right and left ventricles 108, 112 contract to pump blood throughout the body as discussed above.
Normally, the muscular walls of each chamber of the heart 100 contract synchronously in a precise sequence to efficiently circulate the blood as described above. In particular, both the right and left atriums 106 and 110 contract and relax synchronously. Shortly after the atrial contractions, both the right and left ventricles 108 and 112 contract and relax synchronously. Several disorders or arrhythmias of the heart can prevent the heart from operating normally, such as, blockage of the conduction system, heart disease (e.g., coronary artery disease), abnormal heart valve function, or heart failure.
Blockage in the conduction system can cause a slight or severe delay in the electrical impulses propagating through the atrioventricular node 122, causing inadequate ventricular contraction, relaxation, and filling. In situations where the blockage is in the ventricles (e.g., the right and left bundle branches 126 and 128), the right and/or left ventricles 108 and 112 can only be excited through slow muscle tissue conduction. As a result, the muscular walls of the affected ventricle (108 and/or 112) do not contract synchronously (known as asynchronous contraction), thereby reducing the overall effectiveness of the heart 100 to pump oxygen-rich blood throughout the body.
Various medical procedures have been developed to address heart disorders. In particular, cardiac resynchronization therapy (“CRT”) can be used to improve the conduction pattern and sequence of the heart 100. CRT involves the use of an artificial electrical stimulator that is surgically implanted within the patient's body. Leads from the stimulator can be affixed at a desired location within the heart 100 to effectuate synchronous atrial and/or ventricular contractions. Typically, the location of the leads, or the stimulation site, is selected based upon the severity and/or location of the blockage. Electrical stimulation signals can be delivered to resynchronize the heart, thereby improving cardiac performance.
One important parameter associated with CRT is atrioventricular delay or “AV delay,” which is the programmed time interval between a paced or sensed atrial event and the corresponding paced or sensed ventricular event. Referring to FIGS. 3-7, an example timeline and method are shown for calculating an AV delay.
Referring to FIG. 3, a specific instant in atrial (“A”) and ventricle (“V”) activity is illustrated. For example, the sensing of atrial (“As”) activity and sensing of ventricle (“Vs”) activity during intrinsic heart activity is shown for a single heartbeat. The time As represents when atrial depolarization (or electrical activation) is sensed. The time Vs represents when ventricular depolarization is sensed. The interval between As and Vs is the sensed atrioventricular interval (“AVIs”).
The AVIs can be used to calculate an optimal AV delay for ventricular pacing during intrinsic or sensed atrial contraction (“AVDs”), as shown in FIG. 4, using various techniques. For example, methods described in U.S. Pat. No. 6,144,880 to Ding et al. and U.S. patent application Ser. Nos. 10/314,899 and 10/314,910 to Yu et al., all of which are hereby incorporated by reference in their entireties, can be used to calculate AVDs from AVIs. Equation 1 below generally illustrates one possible relationship between AVIs and an optimized AVDs.AVDs=K1(AVIs)−K2   (1)The constants K1 and K2 may vary depending on the interval measured and patient diversity. See U.S. Pat. No. 6,144,880.
In another example, U.S. patent application Ser. No. 10/352,780 to Ding et al., which is hereby incorporate by reference, describes methods for calculating optimal AVDS. For example, the following equation can be used to calculate an optimal AVDs: AVDs=k1AVRs+k2AVLs, where AVRs is the interval between atrial sense and right ventricular sense, and AVLs is the interval between atrial sense and left ventricular sense.
Referring now to FIG. 5, an embodiment in which the atrium is paced (“Ap”) is illustrated. Ap represents the introduction of an electrical impulse to the atrium, and, as previously noted, Vs represents sensing of intrinsic ventricular activity. The interval between Ap and Vs is the atrioventricular interval during atrial pacing and ventricular sensing (“AVIp”).
As shown in FIG. 6, a difference between AVIs and AVIp, labeled as the offset, can be calculated using Equation 2.offset=AVIp−AVIs  (2)Using this offset, the optimal atrioventricular delay for atrial and ventricular pacing (“AVDp”) can be calculated using Equation 3.AVDp=AVDs+offset  (3)
Referring now to FIG. 7, using Equations 2 and 3 described above, an example method is shown to calculate the AVDp for a CRT device. In operation 310, the AVIs is measured by the CRT device. In operation 320, the optimal AVDs for sensed atrium and paced ventricle is calculated as described above. Then, in operation 330, the atrium is paced for one or more beats. In operation 340, the AVIp is measured. Next, the offset is calculated in operation 350 using Equation 2 above. Finally, in operation 360, the optimal AVDp for paced atrium and paced ventricle can be calculated using Equation 3.
Other methods can also be used to calculate an optimized AVDp. For example, U.S. patent application Ser. No. 10/243,811 to Ding et al., which is hereby incorporated by reference in its entirety, describes a method to calculate AVDp using AVIp, according to the following Equation 4.AVDp=K1(AVIp)−K2  (4)
The above example methods illustrated in Equations 1-4 allow for the calculation of AVDs or AVDp using a fixed atrial sensing or pacing rate. A typical pacing system uses a standard pre-set AV delay when pacing a heart. Therefore, prior art systems do not account for changes in atrioventricular delays associated with changes in heart rate or pacing rate, or changes in the mode in which the heart is being paced (e.g., changes from atrial sensing to atrial pacing).
However, optimal AV delays can vary depending on the rate of pacing and on whether the atrium is being sensed or paced. For example, as illustrated in FIGS. 4 and 6, AVDs is usually shorter than AVDp because when pacing the right atrium, activation of the left atrium is further delayed. In order to maintain the appropriate contraction sequence of the left atrium and ventricle, the timing of left ventricular stimulation needs to be delayed correspondingly, which necessitates a longer AVDp.
The AV delay can have a significant impact on the hemodynamic efficiency of the heart 100. AV delays of greater than or less than optimal length can cause asynchronous contraction, which can result in less oxygen-rich blood being pumped during each stroke of the heart 100.
Therefore, there is a need for systems and methods that can efficiently and accurately optimize AV delay, and utilize these AV delays at different sensing and pacing rates and during different pacing modes (e.g., atrial sensing or atrial pacing).